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亚致死性缺血改变犬心脏的心肌抗氧化活性。

Sublethal ischemia alters myocardial antioxidant activity in canine heart.

作者信息

Hoshida S, Kuzuya T, Fuji H, Yamashita N, Oe H, Hori M, Suzuki K, Taniguchi N, Tada M

机构信息

First Department of Medicine, Osaka University School of Medicine, Japan.

出版信息

Am J Physiol. 1993 Jan;264(1 Pt 2):H33-9. doi: 10.1152/ajpheart.1993.264.1.H33.

Abstract

We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared with that of the nonischemic myocardium (26.7 +/- 0.9 vs. 20.8 +/- 0.9 U/mg protein, P < 0.05). Mn-SOD content increased gradually in the ischemic myocardium after sublethal ischemia, with a peak after 24 h (2.8 +/- 0.1 vs. 2.1 +/- 0.1 microgram/mg protein, P < 0.05). There were no differences in the activity and content of Cu, Zn-SOD between these regions after sublethal ischemia. Activities of glutathione peroxidase and reductase were significantly higher and lower, respectively, in the ischemic myocardium than those of the nonischemic myocardium immediately after repetitive brief ischemia, but no differences between these regions were seen in activities after 3 or 24 h. These results indicate that a brief ischemic insult alters myocardial antioxidant activity not only immediately after but also 24 h after sublethal ischemia.

摘要

我们通过对犬心肌进行4次5分钟的局部缺血和再灌注预处理来检测抗氧化活性。在反复短暂缺血后,缺血心肌中的线粒体锰超氧化物歧化酶(SOD)活性与非缺血心肌相比显著增加(18.7±2.1对14.9±1.0 U/mg蛋白,P<0.05)。虽然在亚致死性缺血3小时后这些区域之间的活性没有差异,但与非缺血心肌相比,缺血心肌的活性在24小时后再次显著增加(26.7±0.9对20.8±0.9 U/mg蛋白,P<0.05)。亚致死性缺血后,缺血心肌中的锰超氧化物歧化酶含量逐渐增加,在24小时后达到峰值(2.8±0.1对2.1±0.1微克/mg蛋白,P<0.05)。亚致死性缺血后这些区域之间的铜锌超氧化物歧化酶活性和含量没有差异。反复短暂缺血后立即,缺血心肌中的谷胱甘肽过氧化物酶和还原酶活性分别显著高于和低于非缺血心肌,但在3小时或24小时后的活性在这些区域之间没有差异。这些结果表明,短暂的缺血性损伤不仅在亚致死性缺血后立即,而且在24小时后都会改变心肌抗氧化活性。

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